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(Hypertension. 2004;43:716.)
© 2004 American Heart Association, Inc.

Editorial Commentaries

From Inflammation to Fibrosis: A Stiff Stretch of Highway

From the Division of Cardiovascular Diseases, University of Tennessee Health Science Center, Memphis.

Correspondence to Karl T. Weber, MD, Division of Cardiovascular Diseases, University of Tennessee Health Science Center, Rm. 353 Dobbs Research Institute, 951 Court Avenue, Memphis, TN 38163. E-mail KTWeber@utmem.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Fibroblast fibrous tissue formation follows an inflammatory cell response that appears at sites of cardiomyocyte necrosis, a "dirty" form of cell death. In replacing these lost cells, such fibrosis preserves the structural integrity of the myocardium. This replacement fibrosis, or scarring, is distinct from a reactive fibrosis that surrounds intramyocardial coronary arteries and which, over time, may extend into the contiguous interstitial space. Absent an inflammatory cell response, such as occurs with cardiomyocyte apoptosis (a "sterile" form of cell death), fibrous tissue does not appear. An abnormal accumulation of type I fibrillar collagen, a stiff structural protein, reduces myocardial distensibility while a pharmacology-based regression of cardiac fibrosis is accompanied by an improvement in diastolic stiffness (reviewed in References ^{1, 2}). It is not the quantity but rather the quality of myocardium that determines its stiffness.

What accounts for reactive fibrous tissue formation involving the vasculature? To address this question the relative importance of hemodynamic factors versus circulating hormones that accompany any experimental model need to be considered. For example, in placing an occlusive band around the abdominal aorta, either above or between the renal arteries or around a single renal artery, the renin-angiotensin-aldosterone system (RAAS) is activated as a result of renal ischemia. The accompanying elevation in arterial pressure is created by the band and RAAS effector hormones. An infusion of either angiotensin (Ang) II or aldosterone (ALDO) is accompanied by arterial hypertension due to multiple mechanisms, which are beyond the scope of this brief commentary. Circulating Ang II and ALDO . . . [Full Text of this Article]

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